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Humans reach their maximum height at around their mid-20s. It is commonly thought that taller people have better life outcomes, and are in general healthier. Though this misconception stems from misconceptions about the human body. In all reality, shorter people live longer than taller people. (Manlets of the world should be rejoicing; in case anyone is wondering I am 5’10”.) This flies in the face about what people think, and may be counter-intuitive to some but the logic—and data—is sound. I will touch on mortality differences between tall and short people and at the end talk a bit about shrinking with age (and studies that show there is no—or little—decrease in height due to self-reports, the study is flawed).

One reason why the misconception of taller people living longer, healthier lives than shorter people is the correlation between height and IQ—people assume that they are traits that are ‘similar’ in that they become ‘stable’ at adulthood—but one way to explain that relationship is that IQ is correlated with height because higher SES people can afford better food and thus be better nourished. Either way, it is a myth that taller people have lower rates of all-cause mortality.

The truth of the matter is this: smaller bodies live longer lives, and this is seen in the animal kingdom and humans—larger body size independently reduces mortality (Samaras and Elrick, 2002). They discuss numerous lines of evidence—from human to animal studies—and show that smaller bodies have a lower chance of all-cause mortality, the reasoning being (one of the reasons, anyway) that larger bodies have more cells which then would, in turn, be more subject to carcinogens and, obviously, would have higher rates of cancer which would then, too, lower mortality rates. Samaras (2012) also has another paper where the implications are reviewed for this, and other causes are proposed for this observation. Causes are reduced cell damage, lower DNA damage, and lower cancer incidence; with other, hormonal differences, between tall and short people that explain more of the variation between them.

A positive linear association was observed between height and cancer mortality. For each standard deviation greater height, the risk of cancer was increased by 5% (2–8%) and 9% (5–14%) in men and women, respectively.

One study suggests that “variations in adult height (and, by implication, the genetic and other determinants of height) have pleiotropic effects on several major adult-onset diseases” (The Emerging Risk Factors Collaboration, 2012). Taller people also are at greater risk for heart attack (Tamaras, 2013). The cause for this, Tamaras writes, is “including reduced telomere shortening, lower atrial fibrillation, higher heart pumping efficiency, lower DNA damage, lower risk of blood clots, lower left ventricular hypertrophy and superior bloodparameters.”Height, though, may be inversely associated with long-term incidence of fatal stroke (Goldbourt and Tanne, 2002). Schmidt et al (2014) conclude: “In conclusion, short stature was a risk factor for ischemic heart disease and premature death, but a protective factor for atrial fibrillation. Stature was not substantially associated with stroke or venous thromboembolism.” Cancer incidence also increases with height (Green et al, 2011). Samaras, Elrick, and Storms (2003) suggest that men live longer than women live longer than men due to the height difference between them, being about 8 percent taller than women but having a 7.9 percent lower life expectancy at birth.

Height at mid-life, too, is a predictor of mortality with shorter people living longer lives (He et al, 2014). There are numerous lines of evidence that shorter people—and people of shorter ethnies, too—live longer lives if they are vertically challenged. One study on patients undergoing maintenance hemodialysis stated that “height was directly associated with all-cause mortality and with mortality due to cardiovascular events, cancer, and infection” (Daugirdas, 2015; Shapiro et al, 2015). Even childhood height is associated with prostate cancer acquisition (Aarestrup et al, 2015). Even men who are both tall and have more adipose tissue (body fat) are more likely to die younger and that greater height was associated with a higher risk of acquiring prostate cancer (Perez-Cornago et al, 2017). Short height is a risk factor for death for hemodyalisis patients (Takenaka et al, 2010). Though there are conflicting papers regarding short height and CHD, many reviews show that shorter people have better health outcomes than taller people.

An additional inch increase in height is related to a hazard ratio of death from all causes that is 2.2% higher for men and 2.5% higher for women. The findings are robust to changing survival distributions, and further analyses indicate that the figures are lower bounds. This relationship is mainly driven by the positive relationship between height and development of cancer. An additional inch increase in height is related to a hazard ratio of death from malignant neoplasms that is 7.1% higher for men and 5.7% higher for women.

[…]

It has been widely observed that tall individuals live longer or die later than short ones even when age and other socioeconomic conditions are controlled for. Some researchers challenged this position, but their evidence was largely based on selective samples.

Four additional inches of height in post-menopausal women coincided with an increase in all types of cancer risk by 13 percent (Kabat et al, 2013), while taller people also have less efficient lungs (Leon et al, 1995; Smith et al, 2000). Samaras and Storms (1992) write “Men of height 175.3 cm or less lived an average of 4.95 years longer than those of height over 175.3 cm, while men of height 170.2 cm or less lived 7.46 years longer than those of at least 182.9 cm.”

Lastly, regarding height and mortality, Turchin et al (2012) write “We show that frequencies of alleles associated with increased height, both at known loci and genome wide, are systematically elevated in Northern Europeans compared with Southern Europeans.” This makes sense, because Southern European populations live longer (and have fewer maladies) than Northern European populations:

Compared with northern Europeans, shorter southern Europeans had substantially lower death rates from CHD and all causes.2 Greeks and Italians in Australia live about 4 years longer than the taller host population … (Samaras and Elrick, 2002)

So we have some data that doesn’t follow the trend of taller people living shorter lives due to maladies they acquire due to their height, but most of the data points in the direction that taller people live shorter lives, higher rates of cancer, lower heart pumping efficiency (the heart needs to pump more blood through a bigger body) etc. It makes logical sense that a shorter body would have fewer maladies, and would have higher heart pumping efficiency, lower atrial fibrillation, lower DNA damage, lower risk of blood clotting (duh) when compared to taller people. So it seems that, if you’re a normal American man, then if you want to live a good, long life then you’d want to be shorther, rather than taller.

Height loss was reported by 57 study members (15%, median height loss: 2.5 cm), with nine reporting height loss of >3.5 cm. However, of the 24 subjects reporting height loss for whom true height loss from age 22 could be calculated, assuming equivalence of heights within 0.5 cm, 7 had gained height, 9 were unchanged and only 8 had lost height. There was a poor correlation between self-reported and true height loss (r=0.28) (Fig. 1).

In this population, self-reported height was off the mark, and it seems like Hsu takes this conclusion further than he should, writing “Apparently people don’t shrink quite as much with age as they think they do.” No no no. This study is not good. We begin shrinking at around age 30:

Men gradually lose an inch between the ages of 30 to 70, and women can lose about two inches. After the age of 80, it’s possible for both men and women to lose another inch.

For both sexes, height loss began at about age 30 years and accelerated with increasing age. Cumulative height loss from age 30 to 70 years averaged about 3 cm for men and 5 cm for women; by age 80 years, it increased to 5 cm for men and 8 cm for women. This degree of height loss would account for an “artifactual” increase in body mass index of approximately 0.7 kg/m2 for men and 1.6 kg/m2 for women by age 70 years that increases to 1.4 and 2.6 kg/m2, respectively, by age 80 years.

So, it seems that Hsu’s conclusion is wrong. We do shrink with age for myriad reasons, including discs between the vertebrae and spine decompress and dehydrate, the aging spine becomes more curved due to loss of bone density, and loss of torso muscle could contribute to the differing posture. Either way, these are preventable, but some height decrease will be notable for most people. Either way, Hsu doesn’t know what he’s talking about here.

In conclusion, while there is some conflicting data on whether tall or short people have lower all-cause mortality, the data seems to point to the fact that shorter people live longer due since they have lower atrial fibrillation, higher heart pumping efficiency, low DNA damage, lower risk for blood clots (since the blood doesn’t have to travel too far in shorter people), along with superior blood parameters etc. With the exception of a few diseases, shorter people do have a higher quality of life and higher lung efficiency. We do get shorter as we age—though with the right diet we can ameliroate some of those effects (for instance keeping calcium high). There are many reasons why we shrink due to age, and the study that Hsu cited isn’t good compared to the other data we have in the literature on this phenomenon. All in all, shorter people live longer for myriad reasons and we do shrink as we age, contrary to Steve Hsu’s claims.

“Across all cognitive task scores, the general factor accounts for 58.5% of the variance (coefficient omega_hierarchical ωh [102–104]), while group factors account for 18.2% of the variance (with 15.5% of the variance unaccounted for). Another important metric is coefficient omega_subscale ωs [105] which quantifies the reliable variance across the tasks accounted for by each subscale, beyond that accounted for by the general factor; we find ωs cry=38.7%, ωs spd=57.4%, ωs vis=9.9% and ωs mem=27.8%. While some of these subscale factors account for a
substantive proportion of the variance across their respective tasks, their measurement quality is at most fair [44] due to the limited number of constituent tasks; thus we choose to focus onnthe general factor g only. Factor scores are indeterminate, and several alternate methods exist to derive them from a structural model [80]. To avoid this issue, most researchers prefer to remain in latent space for further analyses [41]. However, for subsequent analyses we require factor scores for g, which we derive using regression-based weights (“Thurstone” method). We compare the general factor score derived from this exploratory factor analysis (EFA) with a simple composite score consisting of the sum of standardized observed test scores. As expected, we find that the simple composite score correlates highly with the EFA-derived g
(r=0.91). ”

“The present study is a step in this direction, offering to our
knowledge the to-date most robust investigation specifically focused on predicting intelligence from resting-state fMRI data. Here we used factor analysis of the scores on 10 cognitive tasks to derive a bi-factor model of intelligence, including a common g-factor and broad ability factors, which is the standard in the field of intelligence research [28,44]. We used reliable estimates of functional connectivity in a large sample of subjects, from one hour of high-quality resting-state fMRI data per subject. We used the best available inter-subject alignment algorithm (MSM-All), a stringent control for confounding variables, and out-of-sample prediction. With these state-of-the-art methods on both ends of the tunnel, we demonstrated a strong relationship between general intelligence g and resting-state functional connectivity (at least as strong as the well established relationship of intelligence with brain size [43,44]). We further established that predictive network edges were fairly distributed through the brain, though they mostly fell within 4 of the 7 major resting-state networks: the fronto-parietal network, the default mode network, the control network, and the visual network. These findings are in general agreement with the parieto-frontal integration theory (P-FIT) of intelligence”

I wish I could post the supplementary data. I should note this is not a study of neural efficiency, but instead of functional connectivity. Essentially it is a new and improved PFIT theory. Those same Authors made a nother study on functional connectivity and personality: https://www.biorxiv.org/content/early/2017/11/07/215129

here is another study, on the connection connectivity has with efficiency:

” Analyses reveal evidence that higher intelligence is associated with a lower brain activation (or a lower ERD, respectively) and a stronger phase locking between short-distant regions of the frontal cortex.”

Thanks for the papers. No time to really go through them but I did read Ge (2018) the other day actually. This is an important caveat, so my critiques of GWAS in my testosterone article as well as Ken Richardson’s GWAS critiques still hold here:

Findings in this analysis should be generalized with caution to populations with different sample characteristics with respect to age range, sex composition, ancestry groups, socioeconomic status, educational attainment or other environmental exposures [38].

Also:

Although we identified phenotypic and genetic correlations between fluid intelligence and cortical thickness measurements in several brain regions, these correlations do not necessarily indicate causal relationships. Future work using methods such as Mendelian Randomization may shed light on whether genetic influences on human intelligence are mediated through brain morphology. Also, genetic correlation is a genomewide metric and does not provide any information about specific genes that might underlie both intelligence and brain structure. Further statistical and molecular genetic analyses are needed to dissect their genetic overlap.

Your other reference explains 4 percent of ‘cognitive ability’ differences, and as Richardson writes in his GWAS paper, it’s confounded by social class and social and genetic stratification can explain the relationship with GWAS and cognitive abilities since classes differ genetically and this is functionally irrelevant to cognitive ability and educational attainment.

I’ll review your other cites later, or I just may keep it under wraps and just add it to my piece on g. I also read Kruschwitzab et al (2018) a few weeks back too. Pretty good, covers a few things even though it’s a rebuttal to a specific paper, it talks about other things regarding the brain and efficiency.

See, you can cite all the brain imaging studies in the literature and it won’t mean anything unless 1) specific genes are identified that cause trait variation and 2) the pathways that cause trait variation are identified. This is something, as I’ve stated previously, heritability estimates don’t do so they’re useless. Genes, in the behavioral genetics paradigm, are assumed to work in a certain, additive way but there is no evidence for the assertion. Physiological brain studies don’t show which genes cause anything—if any genes cause this at all (see Richardson’s GWAS critique). Social and genetic stratification can explain these small correlations. It can also explain the differences in brain physiology in these studies since, as I’ve shown, no control for SES or ancestry (this is a UK biobank study and Richardson’s critique is apt).

Which one? if you mean the GWAS study, then that’s expected it’s only measuring one aspect of IQ tests. If you meant the one I quoted, then no, it explained 22% of the variance, which is actually large, and the methodology was extremely robust.

“I also read Kruschwitzab et al (2018) a few weeks back too”

Do you have the full study?

“1) specific genes are identified that cause trait variation and 2) the pathways that cause trait variation are identified. ”

Not really, I don’t expect humans to differ much genetically because of their homogeneity, though I expect vast genetic differences in intelligence compared to chimps. I think the discrepancies between individuals have arisen in the last few thousand years due to developmental plasticity in response to differing environments(Epigenetics). I don’t think the discrepancies are easily “fixable” neither does this mean they lack heredity. The GWAS was not evidence for my point, I simply wanted your opinion because I know you’re skeptical of them.

Which one? if you mean the GWAS study, then that’s expected it’s only measuring one aspect of IQ tests. If you meant the one I quoted, then no, it explained 22% of the variance, which is actually large, and the methodology was extremely robust.

No it’s to be expected because of socioeconomic class and genetic stratification. That explains the low correlations regarding GWAS studies. The explanation for low variance explained is the sample size isn’t high enough but the estimates keep getting higher and higher and we don’t find anything because they use a flawed paradigm.

Not really, I don’t expect humans to differ much genetically because of their homogeneity, though I expect vast genetic differences in intelligence compared to chimps. I think the discrepancies between individuals have arisen in the last few thousand years due to developmental plasticity in response to differing environments(Epigenetics). I don’t think the discrepancies are easily “fixable” neither does this mean they lack heredity. The GWAS was not evidence for my point, I simply wanted your opinion because I know you’re skeptical of them

What do you mean ‘not really’? That’s how this is done. You need to identify genes, then identify how these genes cause differences in trait variation then which pathways the trait variation occurs I’m not worried about whether so-called discrepancies can be ‘fixed’, so much as they have flawed methodology and are based off of outdated models of the gene along with their flawed assumptions.

“Why don’t you know? It’s the last reference you previously provided.”

I thought it was an abbreviation for something, not his last name.

“No ”

Yes, I didn’t say anything wrong. If you split g into multiple parts the variance will be lower, that’s a mathematical inevitability.

“What do you mean ‘not really’? That’s how this is done. You need to identify genes, then identify how these genes cause differences in trait variation then which pathways the trait variation occurs I’m not worried about whether so-called discrepancies can be ‘fixed’, so much as they have flawed methodology and are based off of outdated models of the gene along with their flawed assumptions.”

Not really as in I don’t need to meet that criteria for validation, that is not how it’s done. Genetic variation is not needed for phenotypic variation, and since humans are so incredibly homogeneous, I highly doubt discrepancies are rooted in mutational/genotypic differences. It’s pathetic I have to explain this to you, seeing as how you preach lamarckism all day.

Yes, I didn’t say anything wrong. If you split g into multiple parts the variance will be lower, that’s a mathematical inevitability.

‘Multiple parts’? No. The explanation most commonly given is that the n isn’t high enough to have sufficient power to detect larger variation. And I am arguing that the low variance explained (4 percent in the Dubois preprint) is all due to social class. I’ve provided argumentation and citations for that specific claim.

Genetic variation is not needed for phenotypic variation, and since humans are so incredibly homogeneous, I highly doubt discrepancies are rooted in mutational/genotypic differences.

No shit. And most genetic variation is irrelevant. Most traits important for survival are canalized in development or taken into developmental plasticity. And so, natural selection lowers heritabilities by eliminating deleterious alleles which is why IQ heritability should be much lower than it is (from the flawed twin studies) and is why IQ heritability estimates “far surpass anything seen in the animal kingdom” (Schonemann, 1997). Low heritabilities also don’t mean low genetic variation, just that phenotypic variation has little correlation with phenotypic variation.

The point of talking about genes that cause trait differences and knowledge of which pathways cause trait variation has nothing to do with Lamarckism.

You’re a pseudo-intellectual, where did I say you were wrong? All I did was add perspective. Point it out right now. Yes “multiple parts’ as In fluid, and crystallized.

You said that “If you split g into multiple parts the variance will be lower, that’s a mathematical inevitability.” well I pointed out that that’s not why the explained variance is so low and I’ve never come across that type of argument from people who do GWAS studies. The explanation is that the n is too low, but I’ve shown that GWA studies show genetic class differences that are functionally irrelevant to cognitive ability and educational attainment. Crystallized and fluid ‘intelligence’ are irrelevant to GWAS studies.

You literally learned this a couple weeks ago. I’ve known it for 4 years.

You literally have no idea of knowing that at all. You’re wrong. I know more biology than you, Mr “didn’t know what ATP was and thinks he knows more biology than my University biology professor”.

My point being I don’t need to demonstrate Genotypic differences that correspond with intelligence, because there probably aren’t any(that have a significant effect).

Why not? There should be, especially mediating the differences found in the P-FIT areas of the brain…

“well I pointed out that that’s not why the explained variance is so low ”

Did I ever say you were wrong? No, reading comprehension.

“Crystallized and fluid ‘intelligence’ are irrelevant to GWAS studies.”

Reading comprehension. The study was specifically looking for genetic variation on fluid intelligence.

“You literally have no idea of knowing that at all.”

Yes I do, otherwise you would not be promoting this nonsense with such naive enthusiasm.

“You’re wrong. I know more biology than you, Mr “didn’t know what ATP was and thinks he knows more biology than my University biology professor”.”

Well you have yet to demonstrate this. In fact, through out our conversations you’ve shown a startling lack of knowledge on the subject. For example, you don’t know what feedback loops are, you assume individual differences should accompany genetic ones(which indicates you don’t understand heredity) and that’s quite pathetic, because you’ve been propagating epigenetics, which means you don’t understand that either. You have some knowledge, but it’s quite evident you don’t think about it on a deep enough level and just take a lot of what you read at face value simply because you want to argue. You’re going to have to try harder if you want anyone to take you seriously.

“Why not? ”

Because as I already stated genotypic variation is not needed to catalyze phenotypic variance. Further evidence of how little you know about biology, I learned that in 10th grade lMAO.

The study was specifically looking for genetic variation on fluid intelligence.

The other GWAS studies show the same exact low ‘variance explained’…

Yes I do, otherwise you would not be promoting this nonsense with such naive enthusiasm.

Just admit you made a wrong assertion. There is no ‘nonsense’. You didn’t know what ATP was before I explained it to you, you must have taken that day off of school in tenth-grade biology.

you don’t know what feedback loops are

Ha. Provide the evidence, if you can’t then retract the statement. No ‘but I don’t wanna look’, you made a claim, now provide said evidence.

you assume individual differences should accompany genetic ones(which indicates you don’t understand heredity) and that’s quite pathetic, because you’ve been propagating epigenetics, which means you don’t understand that either.

I ‘assume’ individual differences ‘should’ accompany genetic differences because that’s the IQ-ist assertion that needs to be disproved (and something that is pushed in their models). It’s clear I know more biology than you, Melo. I know what feedback loops are, I don’t need you to condescendingly tell me that I do not know something (when it’s clear that I understand epigenetics and cell biology as a whole better than you do which can be seen in my MS article), especially when it’s clear I’m more knowledgeable on the subject.

Because as I already stated genotypic variation is not needed to catalyze phenotypic variance. Further evidence of how little you know about biology, I learned that in 10th grade lMAO.

Haha. I asked you the question because I wanted your answer. Should I not press and ask you questions to see what you say? If I ask you a question, does that mean that I do not know the answer? What does ATP do? Does that mean I don’t know what it does?

Either way, the main claims from the BG model is that differences in genes cause differences in individual variation in ‘IQ’, and it is then assumed that genes work in a specific, additive matter. But genes work in a top-down, bottom-up way and also work non-linearly so, therefore, the BG model is wrong because the nature of the ‘gene’ is not what they believe it to be.

Well, if you had decided to take ten seconds of your time to use your brain, you wouldn’t have wasted either of our time with that redundant bullshit.

“Just admit you made a wrong assertion”

There was no wrong assertion, You’ve only just recently been discussing items from the extended synthesis. And if it really took you that long, then that is further proof of your Intelligence or lack thereof.

“You didn’t know what ATP was before I explained it to you”

And you didn’t know what torque equilibrium was, how feedback loops worked, the difference between mental/genetic plasticity, How thermodynamics worked, how heritability works,(and then a had a temper tantrum when pumpkin agreed with me), You didn’t fully understand sociality, or how diet isn’t a selection pressure, Don’t understand how causation works, thinks the health carter formula predicts morphology, etc ad infinium.

Fuck it I could look back to a lot of conversations and probably pick out many instances where i had to spoon feed you information because you had such a hard time grasping it.

‘Provide the evidence”

You Think Culture has more Equalizing power than genetics, Yet you preach dynamism, holism, epigenetics etc. So it becomes utterly confusing how you can even begin to believe the latter. At that point it is obvious you’re being intellectually dishonest or just too stupid to know any better.

“that’s the IQ-ist assertion that needs to be disproved”

You’re debating me, not them. You need to adapt appropriately, it’s one thing if you straw man in a blog post but don’t reflect them onto me when I make my objections.

“especially when it’s clear I’m more knowledgeable on the subject.”

Yeah come back to me when you can at least spell somatotype correctly.

” I asked you the question because I wanted your answer. ”

I’ve answered it plenty of times and still don’t get it. But I expect that from you now.

You Think Culture has more Equalizing power than genetics, Yet you preach dynamism, holism, epigenetics etc. So it becomes utterly confusing how you can even begin to believe the latter. At that point it is obvious you’re being intellectually dishonest or just too stupid to know any better.

No, I don’t. Just because I talk about cultural and psychological tools regarding test-taking, cognitive processing, and the other socio-cognitive affective variables. That’s completely different from the nature/nurture dichotomy because access to these tools dictate one’s ability to take these tests, combined with stress (which affects the vmPFC and hippocampus as I’ve shown previously), numerous ‘cultural/environmental’ reasons exist why people score lower.

you assume individual differences should accompany genetic ones(which indicates you don’t understand heredity) and that’s quite pathetic, because you’ve been propagating epigenetics, which means you don’t understand that either.

I don’t assume this. I am well aware (hell you can even check my blog) of this. Nothing in my blog indicates this, I’ve stated in the past that identical genes do not restrict variation and that there are many other pathways in which traits can arise. Most genetic variation, though, is irrelevant, which I said to you the other day.

Yeah come back to me when you can at least spell somatotype correctly.

I call it that because I can. I’m more knowledgeable on the subject. This is a fact.

See, I bring up the ATP comment because you made some snarky comment that you know more biology than my University biology professor. I proved that wrong by pointing out that you didn’t know what ATP was, which is basic biology that you did not know.

how feedback loops worked, the difference between mental/genetic plasticity, How thermodynamics worked, how heritability works,(and then a had a temper tantrum when pumpkin agreed with me), You didn’t fully understand sociality, or how diet isn’t a selection pressure, Don’t understand how causation works, thinks the health carter formula predicts morphology, etc ad infinium.

This is dumb. You can’t show me that didn’t know “how feedback loops worked”, nor that I don’t know how thermodynamics worked (dumbest thing I’ve ever seen you say, that’s saying something), I know how heritability works (it’s phenotypic variation and I disproved your claim with the paper from Pigliucci), sociality and diet pressure I’ll slightly give to you (only in the fact of fire; finding food is a pressure. See Melo, like an intelligent being I admitted I was wrong, which is more than I can say for you), morphological characteristics are linked to the Heath-Carter somatypes; therefore it does show morphology. The somatype gives a quantified expression of what individual variations in body type and morphology would be.

We can pick up these conversations in the other relevant threads though. I won’t waste any time addressing anything you say about it here so don’t even waste your time addressing this.

RR, you took a Biology 101 class, you literally know less than any of my highschool teachers. You can bring up ATP all you want, but I’ve already demonstrated your lack of knowledge in rudimentary subjects. You took a logic 101 class and i still had to explain why Anselm’s argument was not sound, so it’s blatantly apparent that you don’t learn very well.

“You can’t show me”

You yelling “muh culture” is proof.

” that I don’t know how thermodynamics worked”

You don’t. I demonstrated this.

“I know how heritability works ”

Actually the papers I cited substantiated my claims. Try again.

“morphological characteristics are linked to the Heath-Carter somatypes”

Some means body. Type is self-explanatory. My verbiage is not incorrect.

RR, you took a Biology 101 class, you literally know less than any of my highschool teachers. You can bring up ATP all you want, but I’ve already demonstrated your lack of knowledge in rudimentary subjects. You took a logic 101 class and i still had to explain why Anselm’s argument was not sound, so it’s blatantly apparent that you don’t learn very well.

No you haven’t. I never claimed to know more than your high school biology teachers. You claimed to know more than my University professors which I proved wrong with the ATP comment. Anselm’s argument is sound.

You yelling “muh culture” is proof.

No it isn’t. I’ve it’s perfectly in-line with the principles of developmental systems theory. When classes are stratified, they have differential access to cultural and psychological tools. This then causes score variance, not ‘genetic’ differences. Most genetic variation is irrelevant. Form and variation are unpredictable because “in complex adaptable traits, there is no direct mapping from genes to phenotype” (Richardson, 2017: 131).The dynamic system is more responsive to the environment. Cause and effect are lost in developmental complexity. “All forms and variation (and, therefore, potential) is created from the evolved dynamics responding to informational patterns at many levels.” (Richardson, 2017: 134)

No you didn’t. The first law is irrelevant to human physiology. People invoke the first law as proof thst a calorie is a calorie. But saying a calorie is a calorie violates the second law of thermodynamics. (I’m not saying you said that.) That’s the reality of the situation. If a room is getting more crowded, what is causing the room to get crowded?

The definitions of endomorphy, mesomorphy and ectomorphy signify the observed shape and composition of the body. Ectos and Mesos are more likely to have longer appendages than endos. Extreme endos would have shorter appendages; extreme ectos and mesos would have longer appendages. Look at Kenyan distance runners, look at Jamaican and black American sprinters. Further the photoscopic method is a valid way to assess one’s somatype.

You don’t get to decide what cuts it. Truth is in abundance. Even if you properly identify the feedback loop using evidence from the prevalent literature, it’s obviously only been to cure some kind of cognitive dissonance, because you have conveniently ignored Synaptic pruning, and regression to the mean which make any within generation plasticity gain(among adults) negligible.

“The first law is irrelevant to human physiology. ”

Sorry, you don’t have a say on that. Biologic laws are always subject to physical and chemical ones.

“(I’m not saying you said that.)”

Then why are you arguing it with me? Stop being stupid.

“Massimo Pigliucci rebutted it.”

No he didn’t. I showed that on average, Homeodynamic systems have low heritabilities, while simultaneously displaying a mathematical model for Plasticity. My only claim was the heritibility estimates can be crude inference for the plasticity of a trait, and I provided evidence. SO you didn’t understand how heritability worked,

“The definitions of endomorphy, mesomorphy and ectomorphy signify the observed shape and composition of the body.”

They don’t address limb proportion.

“endomorphy, mesomorphy and ectomorphy ” measurements are made through a algorithim consisting of body fat,limb,joint girth, HWR etc. The specific morphologies you are discussing have no relevance outside of meaningless correlations. Africans do not have long limbs because they are mesomorphs/ectomorph, they have long limbs because they live in the tropics.

We can discuss ‘what I didn’t properly address’ elsewhere because that has no bearing on this conversation.

Synaptic pruning, and regression to the mean which make any within generation plasticity gain(among adults) negligible.

How do you know it becomes ‘negligible’? Synaptic pruning is evidence for differences in IQ between individuals/groups?

Sorry, you don’t have a say on that. Biologic laws are always subject to physical and chemical ones.

The First Law always holds but it’s irrelevant to human physiology. Physics is physics; physiology is physiology. The First Law has no bearing on weight loss; it just tells us what happens if that thing does happen.

No he didn’t.

Yes he did, and he provided the rationale of het estimates not being useful as well.

They don’t address limb proportion.

Endos have shorter arms; ectos and mesos have longer arms. This is a fact. Just because the Heath-Carter formula does not talk about limb length does not mean you cannot infer limb length from the somatype.

Africans do not have long limbs because they are mesomorphs/ectomorph, they have long limbs because they live in the tropics..

In the northern region of Trento, for example, the average life expectancy is 83 years (81.2 for men and 85.8 for women), while the average Campanian resident can expect to live just 80 years (78.3 for men and 82.8 for women).

[…]

Another problem facing Italy’s healthcare system is the increase in chronic diseases, which affect four in ten Italians, Osservasalute said. These illnesses include, for example, diabetes, obesity, and high blood pressure.

And chronic diseases are not only affecting more Italians than ever, but they are affecting people from is an increasingly young age, a phenomenon which Ricciardi said “lowers quality of life and leads to increasingly unsustainable costs for the health service”.

Of course I agree that it should not be a disease but one should be monitored if his brachial BP is high. Most heart problems concentrated in taller people:

A variety of CVD problems are related to having a taller height. These include: higher blood pressure, greater left ventricular hypertrophy, increased work load on the heart, atrial fibrillation, blood clots and lower heart pumping efficiency (Samaras, 2013). The lower heart rate of taller people is considered a longevity advantage; however, centenarians are usually small with higher heart rates, which conflicts with the slow heart advantage.